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Corticosterone administration and high-energy feed results in enhanced fat accumulation and insulin resistance in broiler chickens.
Br Poult Sci. 2008 Jul; 49(4):487-95.BP

Abstract

1. Two experiments were conducted to investigate the effects of exogenous corticosterone administration (30 mg/kg diet) and dietary energy level on feed or energy intake and fat deposition in broiler chickens of 1 and 4 weeks of age. 2. Corticosterone treatment significantly suppressed body weight (BW) gain and reduced feed and caloric efficiencies. The retarded growth may conceal the stimulatory effect of corticosterone on feed consumption or metabolisable energy (ME) intake. A high-energy diet may increase energy intake and partially alleviate the suppressing effect of corticosterone on growth of broilers. 3. Corticosterone administration promoted the conservation of energy stores as fat at both abdominal and subcutaneous sites and this process occurred regardless of dietary energy level in ad libitum feeding status. A high-energy diet increased fat accumulation and showed no significant interaction with corticosterone treatment. 4. The suppressed development of breast and thigh muscles by corticosterone treatment was observed only in 1-week-old chickens fed on the low-energy diet. In contrast, the yield of breast muscle but not thigh muscle was significantly decreased by corticosterone in 4-week-old chickens, suggesting that the tissue specificity to corticosterone challenge is age dependent. 5. Plasma concentrations of glucose, insulin, triglyceride, non-esterified fatty acids (NEFA) and very low density lipoprotein were increased by corticosterone treatment regardless of diet treatment. A high-energy diet increased plasma levels of NEFA and resulted in hyperinsulinism in 4-week-old chickens but not in 1-week-old chickens. 6. Lipoprotein lipase (LPL) activities in adipose tissues may have been up-regulated by corticosterone treatment and showed tissue specificity. The increased LPL activities at ad libitum feeding status were not necessarily linked with the increased fat accumulation in corticosterone challenged chickens. 7. Corticosterone resulted in augmented energy consumption and altered energy redistribution toward lipid deposition. The induced insulin resistance and enhanced hepatic de novo lipogenesis by corticosterone are likely to be responsible for the increased fat deposition.

Authors+Show Affiliations

Department of Animal Science, Shandong Agricultural University, Taian, Shandong, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18704796

Citation

Yuan, L, et al. "Corticosterone Administration and High-energy Feed Results in Enhanced Fat Accumulation and Insulin Resistance in Broiler Chickens." British Poultry Science, vol. 49, no. 4, 2008, pp. 487-95.
Yuan L, Lin H, Jiang KJ, et al. Corticosterone administration and high-energy feed results in enhanced fat accumulation and insulin resistance in broiler chickens. Br Poult Sci. 2008;49(4):487-95.
Yuan, L., Lin, H., Jiang, K. J., Jiao, H. C., & Song, Z. G. (2008). Corticosterone administration and high-energy feed results in enhanced fat accumulation and insulin resistance in broiler chickens. British Poultry Science, 49(4), 487-95. https://doi.org/10.1080/00071660802251731
Yuan L, et al. Corticosterone Administration and High-energy Feed Results in Enhanced Fat Accumulation and Insulin Resistance in Broiler Chickens. Br Poult Sci. 2008;49(4):487-95. PubMed PMID: 18704796.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Corticosterone administration and high-energy feed results in enhanced fat accumulation and insulin resistance in broiler chickens. AU - Yuan,L, AU - Lin,H, AU - Jiang,K J, AU - Jiao,H C, AU - Song,Z G, PY - 2008/8/16/pubmed PY - 2008/10/28/medline PY - 2008/8/16/entrez SP - 487 EP - 95 JF - British poultry science JO - Br Poult Sci VL - 49 IS - 4 N2 - 1. Two experiments were conducted to investigate the effects of exogenous corticosterone administration (30 mg/kg diet) and dietary energy level on feed or energy intake and fat deposition in broiler chickens of 1 and 4 weeks of age. 2. Corticosterone treatment significantly suppressed body weight (BW) gain and reduced feed and caloric efficiencies. The retarded growth may conceal the stimulatory effect of corticosterone on feed consumption or metabolisable energy (ME) intake. A high-energy diet may increase energy intake and partially alleviate the suppressing effect of corticosterone on growth of broilers. 3. Corticosterone administration promoted the conservation of energy stores as fat at both abdominal and subcutaneous sites and this process occurred regardless of dietary energy level in ad libitum feeding status. A high-energy diet increased fat accumulation and showed no significant interaction with corticosterone treatment. 4. The suppressed development of breast and thigh muscles by corticosterone treatment was observed only in 1-week-old chickens fed on the low-energy diet. In contrast, the yield of breast muscle but not thigh muscle was significantly decreased by corticosterone in 4-week-old chickens, suggesting that the tissue specificity to corticosterone challenge is age dependent. 5. Plasma concentrations of glucose, insulin, triglyceride, non-esterified fatty acids (NEFA) and very low density lipoprotein were increased by corticosterone treatment regardless of diet treatment. A high-energy diet increased plasma levels of NEFA and resulted in hyperinsulinism in 4-week-old chickens but not in 1-week-old chickens. 6. Lipoprotein lipase (LPL) activities in adipose tissues may have been up-regulated by corticosterone treatment and showed tissue specificity. The increased LPL activities at ad libitum feeding status were not necessarily linked with the increased fat accumulation in corticosterone challenged chickens. 7. Corticosterone resulted in augmented energy consumption and altered energy redistribution toward lipid deposition. The induced insulin resistance and enhanced hepatic de novo lipogenesis by corticosterone are likely to be responsible for the increased fat deposition. SN - 1466-1799 UR - https://www.unboundmedicine.com/medline/citation/18704796/Corticosterone_administration_and_high_energy_feed_results_in_enhanced_fat_accumulation_and_insulin_resistance_in_broiler_chickens_ L2 - https://www.tandfonline.com/doi/full/10.1080/00071660802251731 DB - PRIME DP - Unbound Medicine ER -